PCOS and hypothalamic amenorrhea are two specific, different diagnoses. Most medical professionals would never dream of diagnosing a patient with both. Nevertheless, my research, personal experience, and work with clients have demonstrated without doubt that millions of women suffer from both.

PCOS and Hypothalamic Amenorrhea: Why People Think They’re So Different

The majority of women who have PCOS fit into a particular category, and most medical professionals lump all women with PCOS into this category.

For this reason, PCOS typically is understood as a condition of excess.I describe this in great depth in my post on The Causes of PCOS, and also in my manual for overcoming PCOS – PCOS Unlocked. For them, PCOS means being overweight, means high insulin levels, and means high testosterone levels. Other hormone levels might be elevated, too.

For women who fit the PCOS norm, inflammation, overeating, and high hormone levels are considered a problem – thus the idea of excess.

Unfortunately, there are millions of women who suffer from PCOS but who are not quite in the same state of excess. I’ll talk about them (I am one of them) in the sections below.

On the other hand, hypothalamic amenorrhea is typically understood as a condition of scarcity.In hypothalamic amenorrhea, women tend to be very thin, tend to undereat, tend to overexercise, and tend to have very low hormone levels.

For these women, their hormone problem is that they do not produce hormones. Their bodies believe that they are starving, so they shut down reproductive function. This is an evolutionary adaptation. It is potentially life-threatening to be pregnant in a state of famine. To protect against that threat, the female body shuts down when it thinks it may be starving. This is what happens to women and girls with hypothalamic amenorrhea.

PCOS and Hypothalamic Amenorrhea: Why They are Not So Different

PCOS is complicated. It’s an easy diagnosis, but the causes of it are rarely understood. This is because cysts crop up under a wide variety of hormonal circumstances. We might think that this would mean that the medical community recognizes the need for diverse treatment among PCOS patients, but actually it does not. Instead of considering the wide variety of PCOS needs, many doctors (especially those who are not endocrinologists) use blanket diagnoses and treatments for all of their PCOS patients.

The current understanding of PCOS is flawed in two major ways. First is what I just described above. The second flaw is a corollary of that nearsightedness: most members of the medical community (though there is a real debate getting off the ground) believe that it is impossible to have both PCOS and hypothalamic amenorrhea at the same time.

I disagree.

The belief in problem number two, ie, that HA and PCOS are incompatible, derives from the first problem, ie– the lack of a nuanced understanding of PCOS. PCOS is widely regarded as a problem of insulin resistance and being overweight. These are two significant factors that generate cystic ovaries. But they are not the only ones. Only 60 percent of PCOS patients are overweight. Some normal weight PCOS patients are also insulin resistant. Yet others still are not. What causes normal weight women to develop cystic ovaries? And what about insulin-sensitive women?

PCOS and Hypothalamic Amenorrhea: How to Be Different

Each woman needs to have two of the following three characteristics in order to be diagnosed with PCOS:

-Cystic ovaries, as detected via ultrasound

-Elevated male sex hormone (like testosterone) levels

-Irregular or absent menstruation

The thing is that these symtpoms indiciate that the process of menstruation is not completed properly. They indicate that there is an imbalance between male and female sex hormones in the body. The condition of excess of insulin and testosterone I mentioned above is one way to make that happen. It is, however, by no means the only way.

The dominant pathway by which women develop poly cystic ovaries is, again, that of the overweight woman. It is a fairly simple process:

1) insulin stimulates testosterone production in the ovary, and

2) excessive testosterone production throws a wrench in the menstrual cycle.

In PCOS, testosterone and female sex hormones become improperly balanced, and the rest of the menstrual cycle, which takes its cues from the rise and fall of estrogen levels, suffers. LH and FSH, two pituitary hormones that tell the ovaries what to do and when, are of particular concern. LH and FSH levels become dysregulated with dysregulated estrogen because they take their cue from blood estrogen concentrations. This is why the vast majority of PCOS patients have a reversed and high LH and FSH ratio compared to healthy women. The pituitary gland keeps trying to make the body ovulate, but it does not read estrogen signals properly, and the ovaries do not hear the pituitary properly. So these are the markers of the typical PCOS diagnosis: inverted LH and FSH, insulin resistance, overweight, and elevated testosterone levels.

Yet there are other means by which a woman’s hormonal profile can create cysts. One is hypothyroidism (which you can read about and it’s relationship with PCOS in the blog post here).

Today, the problem of primary concern for us is hypothalamic amenorrhea.

PCOS and Hypothalamic Amenorrhea: How to Have Both

HA is known by many to be exactly the opposite of PCOS. It’s a condition of hormonal scarcity.

If hormones are scarce, however, they can still be out of balance.

Most medical professionals consider PCOS a condition of excess. But it is in fact a condition of imbalance. PCOS arises when male sex hormones are elevated over female sex hormones in the body. This can happen when testosterone goes too high — as is the case with the “normal” PCOS patient (though there really is no such thing) — but it can also happen when DHEA-S, another male sex hormone, rises, or when estrogen, progesterone, LH, and FSH drop.

Hormone levels tend to drop in conditions of scarcity.

The body interprets stress, eating too few calories, exercising too much, and having too little body fat as indicators of starvation and scarcity.

Hormones can be imbalanced with the condition of scarcity in a number of ways. I list a few examples below.

PCOS and Hypothalamic Amenorrhea: Examples of having both

-A woman is really stressed out by work and life. While most of her hormone production plummets, her DHEA-S production (the top-of-the-food-chain hormone produced by the adrenal gland) skyrockets in response to HPA axis dysregulation. DHEA-S is an androgen, and it influences the development of cystic ovaries if estrogen levels are not equally as high.

-A woman is fairly healthy but has slept poorly throughout her entire life. This pushes her towards insulin resistance, but more than that it dys- and up-regulates her cortisol production. Cortisol signals to the HPA axis to decrease pituitary activity, and it does so. Her hormone levels all decrease. This woman’s predisposition to insulin resistance coupled with adrenally-induced fluctuations triggers the development of ovarian cysts.

-A woman is stressed out via the typical HA pathways–caloric restriction, excess exercise, and stress–so her pituitary hormones decrease in potency. Testosterone and estrogen levels are low but okay, and the woman is probably thin but may also be larger, depending on the degree of stress. Nevertheless, this time it is progesterone that takes the largest hit from the stress (taking it’s cue from both estrogen and LH), and menstruation can never occur without sufficient progesterone levels.

-A woman has a tendency towards insulin resistance, and is overweight, and then loses weight. While this corrects the insulin problem, the drop in estrogen levels she experiences from the weight loss (since estrogen is produced in fat cells) causes an imbalance in her predisposed-to-testosterone-production ovaries.

– Or a similar phenomenon occurs with leptin: In this case, a woman may be a bit insulin resistant, and therefore have a predisposition to testosterone production, but she does not test into a “dangerous” testosterone zone. Instead, her problem lies in the fact that she lost weight, and with it, she lost the potency of her leptin stores. During puberty, each woman’s body adapts to whatever levels of estrogen and leptin she has circulating in her blood at the time (creating a bit of a leptin “set point”). Later in life, one of these women loses weight. As she loses weight, and, significantly, if she is restricting calories or exercising excessively, her leptin (and estrogen) levels drop. The hypothalamus perceives this drop as an indication of a time of famine, and initiates a starvation response, primarily by decreasing the production of sex hormones. In this woman’s case, therefore, estrogen is low, and testosterone may be low to high, depending on the degree of insulin resistance and ovarian malfunction, but LH and FSH are both also low. She does not present with typical PCOS. She does not over-producde hormones, but, instead, under-produces.

-A woman has the MTHFR gene mutation, which predisposes her to high stress hormone levels, inflammation, and high testosterone levels, but which does not change her female sex hormone levels. When she experiences weight loss or a low body weight, it easily tips the body into a state of imbalance.

All that said, these are some examples of how typical HA problems can cause the cystic condition that is typically associated solely with PCOS. Stress, excess exercise, restricted macronutrient intake, restricted calories, and weight fluctuation can all contribute to cyst development. Many of these situations can co-occur, and that totally depends on a woman’s genetics, epigenetics, lifestyle, and diet.

PCOS and Hypothalamic Amenorrhea: Recommendations

The problem with having a poorly-nuanced understanding of PCOS lies in the way in which blanket recommendations are made for women with PCOS or HA. As a result of this mindset, I have been criticized for recommending that thin women with PCOS eat carbohdyrates. This is because those who are criticizing me believe that PCOS is solely a result of insulin resistance. I do not believe so. I believe that many women with PCOS do not necessarily have a problem with insulin resistance, and even if they do, it can be compounded by factors that lie outside of that typical diagnosis.

I would, then, tentatively recommend that women who are overweight and insulin resistant follow the typical PCOS protocol and under-take insulin sensitizing and gut healing steps. On the other hand, I would tentatively recommend that potentially under-weight and overly-stressed women with PCOS consider eating more, possibly upping their carbohydrate intake, and exercising less. Women with low thyroid would do well to correct that problem however they see fit. This is, however, particular to the individual, so please do not take my musings about PCOS etiology and treatment as prescriptions. Each woman’s experience of PCOS is unique and requires individual troubleshooting.

There are many different causes of PCOS, and it is rare for a woman to only experience one of them. The key to overcoming PCOS is to figure out what is causing your PCOS, and then experimenting with treatment options.

I have written an info-packed, multimedia resource for you, precisely to show you my method for overcoming PCOS with my clients. I also happened to use this method myself, as I was one of the women who has both PCOS and HA (But not anymore!). You can read all about that and get started on your own PCOS today.

I spend a disproportionate amount of my time telling women to eat carbohydrates.

In the paleosphere, it is incredibly common to eat a low carbohydrate diet. Plenty of people use low carbohydrate diets to lose weight, to sharpen insulin sensitivity, and to reduce appetite in the short term.

On the other hand, low carbohydrate diets can be a significant tax on people, women especially.

Because low carbohydrate diets are so popular for weight loss, it is common for women trying to lose weight and to “look good” to exercise often, eat very few carbohydrates, fast, and restrict food intake. The more of these restrictions a woman undertakes at once, the more and more her body reads this as living in a starved, stressed state.

The effects of this are significant: adrenal glands work overtime, livers get tired from performing so much gluconeogenesis, insulin sensitivity drops, body fat levels fluctuate, sleep quality decreases, and libido and fertility decrease.

The problems that come from a low-carbohydrate diet of course don’t affect every woman. Each of us is different. But women who experience stalled weight loss, low-thyroid symptoms, menstrual dysregulation, sleep and or mood and mental health related issues may find significant relief from adding carbohydrates back into their diets.

Many women, contrary to popular paleo belief, in fact lose weight once they add carbohydrates back into their diets. This is because the carbs help the body produce more T3.

(Now, low carb dieters might be quick to point out that the liver can manufacture its own glucose. Certainly, the liver is capable of producing its own glucose with gluconeogenesis, but that process can become taxed over time, particularly if the liver is already taxed from poor eating habits in the past, mineral deficiencies, stress, or calorie restriction.)

-Glucose elicits an insulin response, which in turn spikes leptin levels in the blood.

This is a short-term spike, so eating carbohydrates should not be used as a replacement for body fat, which is the primary long-term secretor of leptin.

However, moderate, regular consumption of carbohydrate spikes leptin frequently enough to help signal to the hypothalamus that the body is being fed. Leptin is absolutely crucial for reproductive function. Without leptin, the hypothalamus does not tell the pituitary to produce sex hormones, so it doesn’t.

–Insulin is also an important signaler of the “fed” state.

In addition to leptin, the hypothalamus also responds to insulin. These two hormones are largely responsible for the female body determining whether it is in a “fed” state.

Being in a fed state is critical for convincing the body it is in a healthy enough environment to reproduce, have a libido, and also lose weight.

Carbohydrate intake boosts tryptophan levels in the brain, and tryptophan is the protein precursor to serotonin. Getting at least some carbohydrate in the diet helps with the vast array of issues associated with serotonin deficiency which include moodiness, stress, and insomnia. People have been shown to sleep better if their dinner includes carbohydrates in it.

This is especially true for women.

For a look at the details and complexities of the issue, see Emily Deans writing here and here. The primary takeaway of this point being that while the exact mechanism of carbohydrates boosting mood and sleep quality is unknown, carbohydrates still appear to be a healthy, and in many cases necessary, macronutrient.

Carbohydrates for fertility and health

The main point here is that carbohydrates are not just okay but important. For women who have appetite control problems, sugar addictions, and a lot of weight to lose, absolutely I believe a low-carbohydrate diet can do them wonders. For women who struggle with menstruation, fertility, stress, exercise performance, or any other hormonal oddities, carbohydrates help assure the woman’s body that she is healthy and fed. This is crucial for reproductive health.

In all cases, diet is a matter of personal physiology and experimentation. If a woman’s body works better on carbs, she should eat them, and delight in those joys rather than worry needlessly. At the very least, they are not harmful, and at their best, they are life saving.

This concept is central to my program Weight Loss Unlocked. If you are interested, it will help you figure out which path to weight loss is best for your unique body and metabolism.

Carbohydrates to eat:

-Starchy tubers such as sweet potatoes, batata, jerusalem artichoke, cassava, tarot, and bamboo. Regular potatoes are fine, too, but they contain fewer vitamins than their sweet counterparts. Of the sweet potatoes, Japanese sweet potatoes are the most delicious, in my opinion, followed by white sweet potatoes and then yams and regular orange sweet potatoes.

These starches are composed primarily of glucose.

–Fruits. All fruits! Berries and cherries tend to have more glucose than fructose, other fruits tend to have more fructose than glucose. This is not a huge point of difference but I have noticed that some women tend to do better on glucose-heavy or fructose-heavy carbs. I personally have an easier time with weight maintenance with fruits than with starches. I talk about this idea more in depth in that Weight Loss program for women I use with my clients.

-Rice Both white and brown rice are fine, but are fairly nutrient-poor.

Brown rice contains anti-nutrients in it’s shell, so white rice is more innocuous in terms of nutrient absorption. Wild rice is another option that I like. Pink rice is something that my friend Noelle from Coconuts and Kettlebells really loves and is a unique way to incorporate rice into the diet! (By the way, if you haven’t listened to The Paleo Women Podcast featuring myself and Noelle, you need to! We are the BEST and we will explain to you ALL THE THINGS. Find us here!)

-Vegetables of course are great, but they do not count for carbohydrate consumption. I know that most of the carbs in vegetables are glucose, but much of it them are also tied up in fiber, which is broken down and turned into short-chain fatty acids by gut bacteria. For this reason, vegetables alone cannot make up a woman’s carbohydrate consumption. Instead, starchy tubers and fruits work the best.

How much carbohydrate to eat for women:

For a woman recovering from stress, metabolic distress, and hypothalamic amenorrhea, I recommend eating between 100-200 g/day. That goes for athletes as well. And for pregnant women. At least 100 g/day.

I typically recommend that women start with 100 grams of dense carbohydrate like starches and fruits and experiment from there. You can definitely eat more than that – I know that I do. But you could also eat a bit less, especially if you prefer a lower carbohydrate appraoch to health.

Remember, you do not necessarily need to eat high carbohydrate. You can, but you don’t have to. It is only that a diet with at least some carbohydrates can really help with fertility, hormone balance, thyroid, and weight loss problems.

The volume of emails I receive from women who start having menstrual problems on a paleo diet is staggering. It is not an enormous volume, no. But it is enough to give a woman pause. What gives? Aren’t we supposed to be healthier on a paleo diet?

Yes, we are, and really, we are. In the vast majority of women who eat a Standard American Diet, specifically those who are overweight, a paleo diet does wonders for balancing hormone levels. It is usually only when a paleo/whole-foods diet is coupled with restrictive norms that women start running into problems. Too little food, too much exercise, and too much stress are really what it all boils down to. The whole foods are not to blame– not in the slightest. What are to blame, instead, are the obsessive ways in which people interact with these foods.

There are several mechanisms that may be at play in the physiology, depending on each woman’s genetics and how each woman undertakes her paleo diet and lifestyle.

What happens in the body when it stops menstruating

The female reproductive system runs off of a sensitive fleet of circulating hormones. When one or several of them is disrupted, many of the others fail at their jobs, too.

During the menstrual cycle, hormone levels in the blood signal to the hypothalamus to signal to the pituitary to release FSH and LH, two hormones that in turn tell the ovaries what to do. FSH–follicle-stimulating hormone– is released in the first part of the menstrual cycle to incite egg development. LH–luteinizing hormone–is released in the second part of the cycle and prepares the endometrium to be shed. Without proper FSH and LH levels, the female body can never convince the ovaries to do their job. FSH and LH are crucial, and they rely on proper functioning of the HPA axis.

This job of the ovaries is to produce the follicles and the eggs, but in doing so it also produces estrogen and progesterone. This fact is important for signalling menstruation, because it is partly the rise and fall of estrogen and progesterone levels throughout the month that signal to the hypothalamus to release FSH and LH at different times. This is, in essence, a circle of signalling. LH and FSH from the hypothalamus to the ovaries, estrogen and progesterone back to the hypothalamus, and so forth.

Hormone malfunctions that cause amenorrhea

–Decreasing estrogen levels stop the pituitary from being able to send out FSH and LH.

–Decreasing leptin levels stop the pituitary from being able to send out FSH and LH. This is because decreased leptin levels signal to the hypothalamus that the woman is lacking energy stores and is, in essence, starving. When the hypothalamus thinks the woman is starving, it puts a halt to normal reproductive functioning. Leptin levels decrease proportionally with fat mass decreases. On the other hand, leptin can also go undetected when an individual is leptin insensitive. Insensitivity is in general a larger problem for overweight women, and low absolute leptin levels are in general a greater problem for thin women.

Both estrogen and leptin are produced in fat cells. These are the two blood serum hormone levels necessary to signal to the hypothalamus that a woman is fed and happy, and that it should go ahead with normal reproduction. Without these two hormones, reproduction ceases. It is well known in the medical literature that the low body fat of anorexic women, models and athletes is what accounts for their amenorrhea. Without fat, a woman simply cannot menstruate.

What is discussed less often in the literature, but is still true (see Wenda Trevathan’s Ancient Bodies Modern Lives) is the fact that a woman’s reproductive system is set up to run on the nutrient basis she has as a young girl. Throughout puberty, if a girl has a higher-than-average or higher-than-healthy body fat percentage, her ovary to hypothalamus signalling may develop as ‘handicapped’ by these fat stores. Because fat cell estrogen is so high, the ovaries do not have to produce as much. For example: If the body’s estrogen set point is 100 units, and fat cells produce 80 units, then the ovaries only need to produce 20 units. Then, if the woman loses weight, the set point remains around 100 or falls a bit to a healthier level (unique to each circumstance), and the fat cells production falls to around 30 units, such that estrogen from the ovaries is then expected to make up for the rest of the estrogen deficit. Many women have no problem with this. Their ovaries jump into higher gear. Many others, on the other hand, do struggle. Their ovaries never end up rising to fill that gap. The thing is– the set point is not stuck precisely at 100. It will decrease to a healthy level. But it might not decrease as far as a woman bent on meeting social expectations of body image is hoping.

The alignment of a woman’s sex hormone levels with the amount of nourishment she has during puberty accounts for why women who live their whole lives on the edge of starvation can still have babies, but women whose body fat percentage decrease from 28 to 21 cannot.

This is not to say that an overweight woman will stop menstruating when she loses weight. Each body is capable of menstruating within the healthiest range of body fat percentages, from around 20 percent to 30 percent. But a woman who has always erred on the side of heavier might find that she cannot dip below 23 or 24 percent body fat without losing her period. 23 or 24 percent body fat is healthy, so this is fine. It might not fly is the woman is trying to meet ridiculous standards of Western body image, but it is optimal for her to have the appropriate serum hormone levels.

Other factors that can hurt estrogen and leptin signalling may also play a role. If a woman can correct those, then she may be able to decrease her body fat levels without hurting her reproductive system. For example, chronic stress hurts hypothalamic signalling. So a stressed out overweight woman is going to have a harder time with reproductive fitness while losing weight than a totally relaxed overweight woman. This is a fact. For menstruation to take place, estrogen and leptin levels must be high enough. Body fat plays a significant role. There are some other factors that can be addresssed and help as well.

Cause 2: Exercise

Weight loss can cause decreased leptin signalling, but exercise can, too. Body fat is the major player in leptin levels, but energy deficiency in general hinders leptin. When a woman is burning more calories than she is consuming–or when she is burning a high quantity of calories while under emotional and physical stress–her body calls it quits. Instead of directing energy towards reproduction, it conserves it for other functions.

Cause 3: Low Calorie Diet

A low calorie diet performs the same function as both weight loss and exercise. It stresses the body and puts the woman in a state of energy deficit. The hypothalamus does not like being in energy deficit, so it tells the ovaries to stop working until it can get itself out of the energy deficit.

A low calorie diet is more of a problem for thin women than it is for women trying to lose weight. Leptin levels first and foremost are reliant on fat stores. The body can eat it’s own fat. That is in fact how weight loss occurs. So if a woman is eating her own fat, she is not starving. Once her body fat levels dip too low, however, and if she is maintaining a low-calorie, starvation-type diet, then she may stop menstruating.

Cause 4: Low Carbohydrate Diet

Many, if not most, women have a real need for carbohydrates. This cause is the most common cause of amenorrhea in the paleo world next to weight loss, in my experience.

Carbohydrates are necessary for the conversion of T4 into T3 (the active form of thyroid hormone) in the liver. The liver is capable of producing its own glycogen when it’s not being fed sugar, but this process can become fatigued over time, especially if the woman is under any kind of stress, or restricting calories, too.

Hypothyroidism, or sub-clinical hypothyroidism, is one of the primary causes of ovarian malfunction. Without sufficient levels of T3, organs shut down, and the reproductive organs are the first ones hit. Without T3, estrogen cannot be produced, and follicles cannot develop. Without T3, a woman cannot menstruate.

For this reason, many paleo women supplement their diets with iodine and find that their amenorrheic symptoms ease. However, many others do not. Instead, they have to add carbohydrates back in to their diets.

Another role that carbohydrates play is spiking leptin levels. Whenever insulin spikes in response to blood glucose, leptin levels rise, too. This means that carbohdyrates help signal to the hypothalamus that the woman is fed. However, this is a short-term elevation. It only spikes in bursts and with meals, so it cannot be used as a long-term solution to health. It is important to note, however, that a high fat, low carbohydrate diet is consistently associated with the lowest leptin levels possible.

Cause 5: High-Dairy Diet (an influence, at least)

Dairy is full of hormones. Even cows raised on pasture cannot help but produce certain hormones that influence a woman’s reproductive system. Dairy is the most androgenic food. It contains a protein that inhibits normal inhibition of testosterone in an individual’s body, such that when someone ingests dairy their testosterone levels can rise unchecked. This is in fact why so many people experience acne when they eat dairy. Even men. It really can increase testosterone levels that much.

Moreover, much of the dairy consumed in today’s world is not organic and grass-fed but is instead choc-full of unnaturally injected hormones. Farms and the US government are touchy about telling the public what goes into their animals, and they claim that these hormone profiles are insignificant. However, anecdotally, myself and with some other women, it seems as though these hormones really can influence women who already have compromised reproductive function. Conventionally raised animals can cause real problems. This goes for dairy, and this goes for eggs and meat products as well.

Cause 6: Altered Phytoestrogen and Hormone-Ingestion Profile

This cause is related to the cause above. We ingest hormones on a regular basis. With a healthy reproductive system, this is not a problem. Hormones from food are far less potent than hormones from the ovaries. Please keep that fact in mind. A healthy reproductive system has very little problem with phytoestrogens in foods. But some women have struggling reproductive systems for one reason or another, and they need to be aware of what hormones they have been and what they are now consuming.

Phytoestrogens are plant estrogens. They look a lot like estrogen, but are not identical. This is why phytoestrogens should never be consumed as a replacement for estrogen. Sometimes they relieve certain symptoms of estrogen-deficiency such as hot flashes, but they also fail to act exactly like estrogen does in the body. This means that other signals and connections are not being made, potentially crucial ones. Hot flashes may cease, but acne may continue to run on unchecked. And other problems can ensue. For example, breast cancer.

Phytoestrogens are primarily in legumes, nuts, and seeds. Soy is the most potent phytoestrogen, and should be avoided at all costs.

There are other sneaky ways in which hormones can infiltrate a woman’s diet, especially if a woman undertakes a paleo diet with compromised reproductive function and inattention to the quality of her food. For example, if a woman goes on an egg-heavy diet when starting paleo, but the chickens are fed a soy rich diet, she is actually eating a soy-rich diet. This is not normally a danger, but with a compromised reproductive system and a soy- or hormonal- influence from poorly treated animal products, it is worth taking into consideration.

These effects, I need to emphasize again, are not usually relevant for women with healthy reproductive systems, and should only be considered in severe cases. Only when hormone levels have dipped so low or have skyrocketed so high that the body becomes sensitive to these normally tolerable and easily managed fluctuations from food. Certainly, conventionally-raised cows are not optimal, but I would not discourage anyone from eating them (in terms of their health) at all if they have no other options. Sincerely. Far, far more important is the quality of hormones being sent through leptin and estrogen signalling within the body.

Cause 7: Stress

The final cause should come as no surprise to anyone. Stress halts reproduction: stress from toxic foods, stress from eating disorders, stress from social life, stress from exercise, stress from work, stress from existential despair… the list is vast. The physiological result of all of the possible stressors is roughly the same, however. Cortisol levels rise and these levels prevent the hypothalamus from sending the appropriate reproductive signals to the ovaries. This may, in fact, be the most important of all the factors I’ve discussed. There is no way to quantify it, and it burns ubiquitously throughout the Western world. What if all of us calmed down? What if we all lived in harmony, and peace, and did not fret? Stress is significant, and stress is real. Hundreds of thousands of American women do not menstruate because they are stressed. How many more experience hindered reproductive function because of stress? I suspect the number lies in tens of millions.

In the first post I wrote on the physiology of women’s weight loss, I focused on the role estrogen plays in fat stores. I noted at the end of the post that estrogen is involved with sending appetite-regulating signals to the brain. This is an important factor in female weight loss. Men have hormonal feedback that dictates their satiation, too, but their body is less attached to how much fat it has. For a woman, having fat is crucial for pregnancy and childbirth. For this reason, a woman’s body errs on the side of caution with respect to fat stores. When in doubt, it screams “eat!” So how is weight loss related to leptin resistance?

What this means is that it is much easier for women to be barraged with physiological demands to eat. These drives are not malicious things, and a woman can never be upset with her body for having them. It’s natural, and it’s necessary for health. Only by accepting our strong biological need for food as physiological fact can we women truly move forward with love, holistic healing, and positive, even pleasurable weight loss.

What follows below is an overview of the mechanisms by which women’s bodies “hang on” to fat stores. This is not to say that the body wants to be overweight. The body wants to be a proper, fit, attractive weight. What happens is that normal weight-regulating factors get dysregulated by an inflammatory diet, and prolonged abuse drives a system further and further off-track. The good news is that because a woman’s body wants to be an appropriate weight, that once a woman starts treating her body with proper love and nourishment, the pounds naturally slide off.

The organ you never knew you had

Not too long ago, scientists thought that fat cells were simple units of energy storage. Metabolism would grab the energy stored in the fat cells when it needed it, and then the fat cells would continue lying there inert. Metabolism might deposit more energy into them at another time, and then later it would come grab the energy back. Fat cells were considered storage units, and not anything more.

Since the discovery of leptin in 1994, science has gradually unearthed the surprising notion that fat tissue is not just a storage space but is also an endocrine organ in and of itself. Fat receives signals from hormones; it is actively involved in how much fat gets stored within its own reserves, and how; and it sends out potent signals of its own. These signals are crucial. They tell the brain how much energy is currently being stored in the form of fat.

Higher levels of leptin signal to the hypothalamus that an organism does not need to eat anymore. Potent appetite stimulators such as neuropeptide Y and anandamide are inhibited by leptin in the hypothalamus, and the production of alpha-MSH, an appetite suppressant, is encouraged. Though there are dozens of hormones and neurotransmitters involved in signaling appetite to and from the brain, what this demonstrates is that leptin runs the show.

More leptin = less eating.

That is, unless the organism is experiencing leptin resistance

Could you be leptin resistant?

Leptin resistance occurs when leptin has flooded a system. In addition to originating in fat stores, leptin levels in the blood rise with food consumption.

1) Leptin spikes after consumption of a large meal, particularly a carbohydrate-heavy meal, since leptin works in tandem with insulin

2) it sort of dribbles into the bloodstream if food is eaten in smaller quantities throughout the day. So leptin levels rise whenever the body really thinks it has been well-fed.

Over-secretion of leptin is the primary means by which people dysregulate their leptin signaling. For example, if they eat too many meals without waiting for hunger to return in between them, or if they graze all day, or if they have a couple of snacks each day. Basically, leptin resistance develops when normal weight-regulating drives are ignored.

Contributing factors of leptin resistance:

Under the influence of these factors it becomes difficult for a woman to hear the leptin signaling in her hypothalamus.

Once people begin ignoring their leptin signals, they get easier and easier to ignore. This is because constantly elevated leptin levels cause leptin receptors to become insensitive to the leptin floating around in the bloodstream. As the body realizes that it’s normal leptin signaling isn’t getting the job done, it incites more eating, more weight gain, and higher leptin levels in hopes that an increased leptin signal will get through. For this reason, obesity is correlated with high leptin levels, even though many obese people complain of constant hunger.

Leptin resistance is a problem for everybody. Both men and women. Without fixing leptin sensitivity problems, it’s very difficult to lose weight. It’s even more difficult to enact any kind of dietary restriction. But women, who have higher levels of leptin than men (having higher body fat percentages) and who have HPA axes more attuned to energy conservation, are particularly sensitive to fluctuations in leptin levels.

Leptin resistance and menstruation

Achieving a certain leptin level is the primary trigger for menarche (the first incidence of menstruation). Stress, genetics, being exposed to smoking, and not being breast fed are other important factors. So far as researchers can tell, throughout evolutionary history a woman’s period likely started around 15 or 16 years of age. A few studies were conducted in the nineteenth century documenting menarche. In 1850, girls began menstruating at an average age of 17; by 1960 that age decreased to 13 years old. Today in America, approximately 10% of girls start to menstruate before 11 years of age, and 90% of all US girls are menstruating by 13.75 years, with a median age of 12.43 years. Both black and Latino girls begin menstruating before white girls.

Leptin and the reproductive set point

Knowing about puberty and menarche is so important for adult women because a woman’s reproductive functioning for the rest of her life is influenced by the conditions of her early reproductive years. Having started menstruation with a certain leptin concentration in the blood, a woman’s body treats this as a “set point ” of sorts later on. This certain level of leptin influences the young girl’s estrogen and progesterone levels, that these also become reproductive set points. If a woman drops too far below her set leptin or estrogen levels later in life by losing too much weight, her body will do its damndest to get those levels back up. A similar phenomenon happens if she becomes overweight and experiences leptin resistance.

Stimulating appetite in response to low leptin levels

The way a body tries to increase leptin and estrogen concentrations is to increase fat mass. The way to increase fat mass is to increase appetite. This is why leptin is such a potent signal in a woman’s brain. With decreased leptin levels (or leptin insensitivity), appetite-stimulating neurons up-regulate powerfully.

Importantly, more women profess sugar addiction than men. One of the neurons that detects decreasing leptin concentrations in the blood is called Neuropeptide Y. Neuropeptide Y stimulates carbohydrate craving. Women who are experiencing starvation– or at least women who’s hypothalama are detecting lower leptin levels than their bodies think is optimal — experience insidious carbohydrate cravings.

Are women stuck in leptin set points?

No. Not necessarily.

The thing is, it’s complicated. A woman’s body will never “want” to be overweight. Women start menstruating at a certain leptin level and at a certain age. Even if this occurs at a very young age, the leptin is still around the same absolute level that another woman might experience, just many years earlier. So her leptin levels, if higher earlier than optimal, still are not shooting through the roof at menarche.

Moreover, if a young girl is overweight when she starts her period, at that time her body is probably fighting for and signaling a desire to lose weight. It’s just not working because some of the signals have been disturbed by poor diet and lifestyle. This woman’s body’s need for and desire to lose weight will persist for the rest of her life. The hormone and appetite pathways are all still in place. They are just begging to be restored to their normal function. All the woman needs to do is listen, and to nourish her body properly. In this way, it will be her partner in weight loss, rather than her adversary.

Unexpected appetite stimulators

Appetite is stimulated via a few other important pathways. They are not limited to women. For example, an individual’s cravings for certain foods increases as a result of nutrient deficiencies. Fluctuating insulin and blood sugar are important. Stress is important. Social conditioning, negative thought patterns, psychological responses to hardship, and body image issues also powerfully stimulate cravings.

Neurotransmitters as appetite stimulators

Perhaps most significant, however, is the relationship between neurotransmitters and food, specifically for women. When serotonin levels drop, cravings, again, particularly for carbohydrates, increase. Serotonin levels can be disrupted by a vast number of problems. These span from nutrient deficiencies to an omega 6 – omega 3 imbalance to poor sleep to obesity to exercise and to stress. Serotonin levels also fluctuate with the menstrual cycle. A drop in serotonin during the luteal phase (the last two weeks) of the menstrual cycle is thought to be by many the dominant cause of PMS. This would explain why many women experience increased cravings for sweets throughout PMS. These are natural, up to a point. But PMS is an extreme fluctuation, and solving the underlying diet and lifestyle factors causing PMS should also decrease the wild swings in cravings that many women suffer throughout their menstrual cycles.

The role of neurotransmitters in appetite deserves several posts of its own. They are forthcoming. For now, it suffices to note that neural mood regulators are strong links between a woman’s reproductive system and her weight regulation mechanisms. Sub-optimal serotonin levels increase carbohydrate cravings.

All that said…

Women come equipped with a system designed to maintain adequate fat mass. If a woman is overweight, it’s because the normal weight regulators she has in place are not receiving the proper nourishment required for effective signaling. Leptin insensitivity and leptin resistance, in the case of an overweight woman, or low leptin levels, in the case of an underweight woman, compel her to eat more. Estrogen, as I noted in a previous post, is also a significant weight-regulator unique to women. It, too, is disrupted with diet and lifestyle. Therefore, with the restoration of the proper functioning of all the underlying mechanisms at work in a woman’s body, specifically with leptin and with estrogen levels, a woman’s weight can slide off. More on that in my upcoming post on the easiest, most natural way (paleo diet! decreased stress! self-love!) for women to lose weight.

Take a look at my latest book Weight Loss Unlocked for my plan to help women lose weight and my book Sexy By Nature for more on all things women’s health, confidence, and self love!

There is a hell of a dichotomy occurring in the Paleo blogosphere this month. 99 percent of the time I am pleased as Pooh stuck up a honey tree, nestled in my esoteric corner of paleo-feminist rage, but every once in a while I wish more people could hear what I have to say. Today is one of those days.

The split I am talking about is not all that nefarious. In most cases, it’s benign and can be ignored. But in general I would like to draw attention to it, because I think there’s a lot going on beneath the surface (and here, the depths are not just Nemo and Dory but are instead people’s lives), and that depth requires speaking to. Immediately.

Mark’s Daily Apple has recently done a beautiful series on the benefits of fasting. I loved it. I learned plenty, as I always do on MDA. The series was well-written and -organized, and in fact I ended up directing people who are unfamiliar with fasting to the site in hopes of swaying their opinions. (So let it be clear: I am not against fasting per se.) Yet Chris Kresser has also done an April “Best your Stress” challenge. Serendipitously enough, it concludes today. And it is exactly what it sounds like: an endeavor to spend 30 days taking practical steps to counteract stress. Chris’s idea was that people often spend 30 days trying to get their diets in line. But what about their stress, and their lives? I couldn’t agree more. This man is a gale of fresh, important ideas.

The reason I say these two Big Themes are at odds is because they are. Fasting is a stressor. Period. Mark Sisson would agree. All people who advocate fasting would agree. But all they ever do is put an asterisk at the end of their posts: *people who are stressed should probably not fast, they say. But why? Who is affected, and how? What can fasting and other forms of restriction do to our brains, and to our lives?

What I want to draw attention to today are little loci that sit on the border of the hypothalamus called Hypocretin Neurons. Hypocretin neurons (also called Orexins–and note that the word “orexin” means “appetite increasing”) were discovered just 14 years ago in 1998, but they have radically altered the landscape of eating neurobiology since then. No, they are not the sole molecules responsible for sleep and waking. Mice that have had these neurons removed still sleep and wake in roughly normal patterns. But they never feel alert, and they never suffer insomnia. And when the neurons are activated, the mice leap into action. Hypocretin neurons wake animals up. This much is certain.

The lack of Hypocretin Neuron signalling is the cause of narcolepsy, while elevated Hypocretin levels induce arousal, elevate food intake, and elevate adiposity. Hypocretin Neurons upregulate the production of molecules down several other pathways, too: these include noradrenergic, histaminergic, cholinergic, dopamine, and serotonergic.

The anatomy of Hypocretin Neurons is also coming into greater light. When are the neurons active? What signals do they receive, and what signals do they produce? Research is beginning to show that Hypocretin Neurons are excited by excitatory synaptic currents and asymmetric synapses with minimum inhibitory input. The fact of asymmetry is important. It means that Hypocretin Neurons are instead always acted upon by mostly uniform – excitatory – signals they receive. Hypocretin Neurons only ever up-regulate and relax. They do not down-regulate. Excitatory signals outnumber inhibitory signals 10:1.

One notable source of excitation is corticotrophin releasing hormone, which suggests that stress activates the activity of Hypocretin Neurons. GABA neurons also create a bridge between Neuropeptite Y, which is the molecule that arguably has the strongest appetite-stimulating effect on the brain, and Hypocretin Neurons (more on Neuropeptide Y later this week). From there, Hypocretin Neurons project to all regions of the brain, including the hypothalamus, cerebral cortex, brain stem, and spinal cord. It seems as though Hypocretin Neurons may act as a nexus of signal input for the appropriate synchronization of various autonomic, endocrine, and metabolic processes.

Food restriction further augments recruitment of excitatory inputs onto Hypocretin cells. This explains the relationship between insomnia and adiposity: because of the easy excitability of Hypocretin Neurons, any signal that triggers their activity, regardless of homeostatic needs, will elevate the need to feed in brain circuits such as the locus coeruleus and the melanocortin system while also promoting wakefulness through activation of noradrenaline-stimulating neurons. Anything that promotes the release of corticotrophin releasing hormone (CRH) such as reduced sleep will further trigger Hyocretin Neuron firing and Appetite. This is a vicious cycle. Hypocretin Neurons play the role both of trigger and of accelerator, taking states of wakefulness, insomnia, stress, and obesity into continual positive feedback loops.

So how does leptin factor in? Hypocretin Neurons express leptin receptors. Moreover, some recent complicated neurobiological work done on mice has shown that injecting them with leptin decreases the activity of their Hypocretin Neurons. What this means is that Hypocretin Neuron activity is stimulated in part by decreasing levels of leptin in the blood, and that increased leptin levels reduce the level of excitation running through Hypocretin Neurons. This is coupled by ghrelin activity, which is also detected by Hypocretin Neurons. Ghrelin, which originates in the gut and is known to stimulate appetite, also excites Hypocretin Neurons. What does feeding do, then, for Hypocretin Neuron excitation? Experiments on mice show that re-feeding restores normal Hypocretin activity, to an extent. Repeated abuse takes longer to recover from, but the simple presence of leptin in the blood normalizes the brains of mice.

Hooray! This is good for fasting, right? So long as one re-feeds appropriately, everything should be fine? Well, yes. In a healthfully functioning individual. But not in a) someone who is both stressed and leptin resistant, since increased leptin levels from the re-feed might not be powerful enough to offset other excitatory pathways b) someone who is currently emerging from yo-yo dieting or caloric restriction c) someone who is dealing with an over-stimulated appetite, d) someone experiencing stress, e) someone who has had a history of insomnia, f) someone who is underweight, since they have low leptin levels, g) anyone who has ever had an eating disorder, particularly bulimia or binge eating disorder or h) anyone with HPA axis or endocrine dysregulation, particularly women, including overt stress, hypogonadism, hypothalamic amenorrhea, hypercortisolism, or hypocortisolism (adrenal fatigue.) I am sure the list is incomplete.

In animals, Hypocretin Neurons serve an important evolutionary function. Arousal is a vital behavior in all species. And normally, Hypocretin Neurons respond quickly to changes in input. But in situations of chronic metabolic or endocrine stress, or of recovering from a stressor, they can lead to hyper-activity and hyper-feeding.

Researchers have long known about the link between leptin, sleep, and obesity. The less someone sleeps, the lower her leptin levels, so the more she eats, and the heavier she gets. Hypocretin Neurons may serve as one of the answers to the question of exactly how that phenomenon comes about. Or at least it plays a role. Because 1) Hypocretins simultaneously stimulate appetite and wakefulness, particularly through orexigenic output of the melanocortin system, and subsequent release of CRH, which activates the stress response, and 2) while Hypocretin Neurons wake us up, they also need to be quiet enough for people to go to sleep.

Finally, I raise the questions: how many disordered eaters have trouble sleeping? How many anorexics, binge eaters, calorie restrictors, exercise-addicts, stressed-out individuals, and very low-carb dieters have trouble sleeping? How many people try intermittent fasting and find that it disrupts their sleep or circadian rhythms? How many people wake up in the middle of the night or early in the morning, even though they still need sleep, but for the life of them feel so awake? Part of that answer lies in blood sugar metabolism, for sure. And in other places. Sleep is a hell of a complex phenomenon. But here– Hypocretin Neurons can become overburdened by excitatory signals. They get hyped up in the face of both decreasing leptin levels and leptin insensitivity. They are upset by restriction, and they are upset by fasting. Hypocretin Neurons demonstrate why so many people have difficulty with their appetite and their sleep. If you find that fasting disturbs your sleep, or that you are suffering disordered circadian rhythms along with stress or appetite problems, do you best to relax your system. Don’t fast. Relax. Exercise less. Reduce stress. Eat more. Put on weight. Eat more carbohydrates. Don’t graze. Increase your leptin sensitivity. And listen to your body.

The literature on sleep and obesity is becoming dense. Lots of things happen to people when they sleep. One of them has to do with appetite regulation, so many researchers are coming to believe that sleep plays a dominant role in today’s vast American Overfeed.

This hunch is supported by striking correlations.

In 1960, a survey of over 1 million people found a modal sleep duration of 8-9 hours. In 2002, polls conducted by the National Sleep Foundation indicated that the average duration of sleep for Americans had fallen to 6.9-7 hours. Recent data indicate that a higher percentage of adult Americans report sleeping 6 hours or less. In 2005, in the US, more than 30% of adult men and women between the ages of 30 and 64 years reported sleeping on average less than 6 hours each night. This decrease in sleep duration has occurred over the same time as the increase in the prevalence of obesity and diabetes.

Leptin has a distinct diurnal and circadian rhythm. It has minimum values during daytime and a nocturnal rise with maximum values during early to mid sleep. The amplitude of the circadian variation averages approximately thirty per cent. Leptin levels rise during the night to suppress appetite while sleeping. Moreover, the reduction of leptin at night spells bad news for the rest of the day: it sets the individual up not just with lower leptin levels in general but also decreased glucose tolerance and an increased craving for carbohydrates.

In order to test the effects of sleep deprivation on leptin production, a number of studies have been conducted. They’re all fascinating, so I have provided a quick review of some of the more revealing studies.

1) Many studies are conducted on people with sleep apnea. Epidemiological studies show that they are heavier than the rest of the population. They have greater rates of diabetes and metabolic syndrome. Yet when their sleep apnea is corrected, these people lose weight naturally, and their metabolisms normalize. This probably has to do both with decreased appetite as well as improved metabolic functioning.

2) In one study at the University of Chicago, doctors measured levels of leptin and ghrelin in 12 healthy men. They also noted their hunger and appetite levels. Soon after, the men were subjected to two days of sleep deprivation followed by two days of extended sleep. During this time doctors continued to monitor hormone levels, appetite, and activity. The end result: When sleep was restricted, leptin levels went down and ghrelin levels went up. Not surprisingly, the men’s appetite also increased proportionally. Their desire for high carbohydrate, calorie-dense foods increased by a whopping 45%.

3) In another study at the University of Chicago, a similar protocol was conducted but men were asked to return a year later for a comparison. For six days they got four hours of sleep — their week of sleep deprivation. The men’s food and activity levels were strictly regulated and hormone levels were taken during the day and while they slept. One year later, the men returned for a six-day study with an 8-hour sleep period, so they served as their own comparison group. The results: After their six-day sleep deprivation period, volunteers had a leptin decrease ranging from 19-26 percent.

4) In another study — a joint project between Stanford and the University of Wisconsin — about 1,000 volunteers reported the number of hours they slept each night. Doctors then measured their levels of ghrelin and leptin, as well as adiponectin, insulin, glucose, a lipid profile, and they also charted their weight. The result: Those who slept less than eight hours a night not only had lower levels of leptin and higher levels of ghrelin, but they also had a higher level of body fat. What’s more, that level of body fat seemed to correlate with their sleep patterns. Specifically, those who slept the fewest hours per night weighed the most.

5) In the final study, young, healthy subjects who were studied after 6 days of sleep restriction where they were allowed four hours in bed. After full sleep recovery, their levels of blood glucose after breakfast were higher in the state of sleep debt despite normal or even slightly elevated insulin responses. The difference in peak glucose levels in response to breakfast averaged was large enough to suggest a clinically significant impairment of glucose tolerance. These findings were confirmed by the results of intravenous glucose tolerance testing.Indeed, the rate of disappearance of glucose post injection was nearly 40 per cent slower in the sleep-debt condition than after recovery, and the acute insulin response to glucose was reduced by 30 per cent.

How fast do leptin levels recover from sleep deprivation?

Leptin levels recover almost as soon as regular sleep is resumed, at least in controlled studies. In the first night. However, these studies occur over a week or two at most. If the sleep deprivation is chronic, it seems to have the same effect as fasting does on leptin. Levels remain low–at least for some time–despite resumption of “normal” sleep or eating. It takes time for the system to re-equilibrate after chronic stressors.

How does stress act on this system?

Stress activates cortisol secretion, but it also stimulates sympathetic nervous system activity. This gets adrenaline running in the system, increases heart rate, and increases blood pressure. These two things increase during both partial and acute sleep deprivation. It is well kown that andrenergic (adrenal-related) receptor activation is suppressive of leptin production, and that leptin is reduced in response to adrenaline infusions. For this reason, whatever dampening that stress puts on sleep negatively affects appetite activity.

There are other downstream effects of sleep deprivation. I’ll cover some of them briefly here, then hopefully return to them each on their own.

1) More cortisol dysregulation. One effect of sleep deprivation is a decrease early evening cortisol levels. Normally at that time of day, cortisol concentrations are rapidly decreasing in order to attain minimal levels shortly before habitual bedtime. Yet in one study the rate of decrease of cortisol concentrations in the early evening was approximately 6-fold slower in subjects who had undergone 6 days of sleep restriction than in subjects who were fully rested. This means, basically, that it takes longer for people who have lost sleep to ramp down from that stress and be able to go to sleep again.

2) Thyroid reduction. In one study, after 6 days of 4-hour sleep time, people experienced a striking decrease in the normal nocturnal TSH rise, and the overall mean TSH levels were reduced by more than 30%.A normal pattern of TSH release reappeared when the subjects had fully recovered. T4 was higher in the sleep-restricted condition than the normal condition, indicating that decreased sleep decreases the body’s rate of conversion from T4 to T3.

3) Growth hormone reduction. The temporal organization of Growth Hormone secretion is also altered by chronic partial sleep loss. The normal single GH pulse occurring shortly after people fall asleep splits into 2 smaller pulses, 1 before sleep and 1 after sleep. With decreased sleep, peripheral tissues are exposed to high GH levels for an extended period of time. GH has anti-insulin-like effects, so an increased overnight exposure to GH negatively impacts insulin sensitivity and glucose tolerance.

So what can you do if your sleep is dysregulated? There are some things that can help with sleep. Of course, if there are underlying issues, those may need to be addressed. A good, whole foods diet like the one I detail in Sexy By Nature can help you with that.

Putting away electronic devices or wearing blue blocking glasses before bed can help melatonin production which will help you fall asleep easier as well.